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A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

This Project

INDRA is developed by indralabs, a part of the Harvard Medical School Laboratory of Systems Pharmacology.

This project, indra_db, is also developed by the indralab team. For more information on how we procure our sources, you can go here. This work was funded by ARO grant W911NF‐15‐1‐0544 under the DARPA Communicating with Computers program.

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Statements

AKT1S1 phosphorylated on T246 activates MTOR. 1 / 1

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"Furthermore, PRAS40 phosphorylation by Akt and association with 14-3-3, a cytosolic anchor protein, are crucial for insulin to stimulate mTOR. -- (From Results Section) Because insulin stimulates Akt-mediated phosphorylation of PRAS40 at Thr 246 (ref. 26), we considered the possibility that PRAS40 phosphorylation may influence insulin activation of mTOR. Both wild-type PRAS40 and mutant PRAS40T246A expressed in 293T cells inhibited S6K1 phosphorylation and this inhibition was reduced on Akt1 coexpression with wild-type PRAS40 but not PRAS40T246A--"

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Our Sources:

INDRA allows us to combine the results from a multitude of sources. In particular, the INDRA Database draws on the following...